Actually, the impairment of these degradation systems promotes an accumulation of misfolded and abnormal proteins, including amyloid-beta (Aβ) in AD, huntingtin (HTT) in HD, superoxide dismutase-1 (SOD1) and TAR DNA-binding protein 43 (TDP-43) in ALS, and α-synuclein in PD [50]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.